To restate:
The patient is a 50 year old woman who admits to “serious drinking” of at least 1 pint of vodka a day for at least 2 weeks. She is admitted looking ill and slightly confused. Her initial labs:
| Electrolyte panel | |||||
|---|---|---|---|---|---|
| Na | 137 | Cl | 89 | BUN | 8 |
| K | 4.3 | HCO3 | 7 | creat | 0.7 |
| Blood Sugar | 55 |
Other labs included an albumin of 4.9, ALT 109, AST 169, alk phos 134, Total bili 1.5
I left the history that she had vomited multiple times over the previous 24 hours.
My thoughts at this point:
Clearly she had an increased anion gap acidosis. I use the mneumonic KILU to teach anion gap acidosis. I do this because this method has physiologic coherence. I can teach concepts rather than a seemingly random list.
The resident did not get an ABG or a serum osm, but the serum did have strong ketones. We assumed alcoholic ketoacidosis.
The patient appeared volume contracted. There are several methods for using the delta gap. I generally add the delta gap to the observed bicarbonate to estimate the “original” bicarbonate. In this patient we must adjust for the albumin of 4.9. Thus, the expected gap is 14-15. Using 14 we have an excess gap of 27 (41-14). Adding the 27 to 7 we estimate the underlying bicarbonate of 34, consistent with a metabolic alkalosis. So we assume metabolic alkalosis secondary to vomiting and volume contraction, alcoholic ketoacidosis, and possibly (although not measured) mild lactic acidosis.
She received aggressive volume expansion and looked significantly better the next morning. However her next BMP gave cause for pause:
| Electrolyte panel | |||||
|---|---|---|---|---|---|
| Na | 138 | Cl | 109 | BUN | 6 |
| K | 3.9 | HCO3 | 17 | creat | 0.6 |
| Blood Sugar | 124 |
What would you do now? What do you think is her problem when you see her on rounds the next morning?
{ 4 comments… read them below or add one }
I imagine one of the things you’ll have to do is replenish her potassium.
I don’t know if that’s the answer but to go to a tangent, what possible rationale is there for not drawing blood gases? In a patient with a bicarb of 7?
The test gives a huge amount of information – far more than virtually any other test in this type of situation (‘m sure she got a U/A and a CBC)
It takes a tremendous amount of guesswork out of the differential gives us an idea of the severity of the problem and how sick the patient might be.
This seems to be the trend- no one wants to draw blood gases anymore – even in cases where they are obviously indicated.
You are an educator -perhaps when you are done explaining this problem – which is after all an acid-base problem, you can explain this trend away from ABGs, which has a secondary effect that residents no longer understand their interpretation. And unlike some diagnostic tests which get superseded by better ones, there are few tests better in sick people than blood gases. What’s going on?
I think I see where you’re going with this:
We’ve corrected the gap but still have an acidosis, thus now she has a normal anion-gap acidosis. When I see this I immediately look to the history for any diarrhea thinking about GI bicarb loss and I look at the PMH and Meds thinking about the three types of RTA’s. I’d probably check urine lytes to calculate the urine anion gap which if positive would tell us the kidneys are not appropriately excreting acid. You can also get a normal anion-gap acidosis secondary to a high volume normal saline infusion, which she had and I’m guessing is the cause. I may not be remembering correctly why this happens, but I think it is the excessive chloride that causes renal bicarb wasting?
The anion gap is gone. You replaced the fluids and the metabolic alkalosis is gone from the vomiting. But your still left with a non gap metabolic acidosis. I suspect this is probably a compensatory response to the respiratory alkalosis your patient experienced while trying to blow off anions for the last two weeks. Now that she isn’t breathing so fast, her CO2 is building up, relative to the delayed kidney response, perhaps giving her a “relative respiratory acidosis”.
A gas would be helpful at this point.
I essentially agree with Happy Hospitalist above. You used the delta gap to estimate that without the ketones/lactate, serum bicarbonate would have been 34. What you have now looks like a non-gap acidosis, which of course could not have co-existed with the metabolic alkalosis you diagnosed when she came in. But what if this isn’t metabolic acidosis, but rather a baseline and pre-existing respiratory alkalosis from her liver disease? The original metabolic alkalosis was simply more severe than you thought. As HH points out, one could test this hypothesis by getting an ABG now, which I would predict will show a pH an the normal range with a low pCO2.
{ 2 trackbacks }